Aging produces deficits in skeletal muscle function, including the loss of mass (sarcopenia) and metabolic capacity. Mitochondrial dysfunction (decreased P/O coupling) is a primary contributor to the changes. Oxidative damage contributes to the dysfunction, although it is unclear where the damage occurs and the specific consequences to mitochondrial function. There is increased incidence of sarcopenia and associated metabolic dysfunction in type-ll (fast, glycolytic) muscle fibers, which may be explained by greater generation of reactive oxygen species and lesser resistance to oxidative damage. The goal of this work is to determine the mechanisms responsible for triggering mitochondrial dysfunction in aging muscle and to determine the mechanistic basis of the dysfunction. This will be tested by identifying oxidative damage to mitochondrial macromolecules, testing the role of uncoupling protein (UCP3), and testing the efficacy of exercise training to reverse mitochondrial dysfunction by driving repair of damaged components. Isolated rat muscles that are either predominantly type-l (soleus) or type-ll (EDL) will be used to test susceptibility of particular fiber types. This work furthers an understanding of aging muscle and allows design of exercise strategies for the elderly.